For many years, scientists believed that asthma was caused mainly by a group of chemicals called leukotrienes.
These molecules are released by white blood cells when something like dust, pollen, or smoke irritates your lungs. Once released, they start a chain reaction that leads to inflammation, narrowed airways, and trouble breathing.
Because of this, most asthma medications today work by blocking the effects of leukotrienes.
But researchers from Case Western Reserve University have made a discovery that could change everything we thought we knew.
A team led by chemistry professor Robert Salomon has found a different type of molecule that may actually be the main cause of asthma attacks. These molecules look like leukotrienes but are created in a completely different way. The team is calling them “pseudo leukotrienes.”
The study shows that these pseudo leukotrienes are formed through a process involving free radicals. Free radicals are unstable molecules that react with oxygen, much like fire reacts with fuel.
This chemical reaction adds oxygen to fats in the body, creating these pseudo leukotrienes. Unlike the leukotrienes that are formed by enzymes in a controlled way, the free radical process is wild and can easily go out of control.
In people with asthma, the body might not have enough antioxidants or enzymes to clean up these free radicals. As a result, more pseudo leukotrienes are formed, which then cause inflammation. These molecules, just like leukotrienes, can “fit” into a receptor in the body—like a key fitting into a car’s ignition—and start the process that narrows the airways.
Current asthma drugs, like Singulair, try to block this ignition by preventing the leukotriene from fitting into the receptor. But if pseudo leukotrienes are actually the ones causing the biggest problem, these drugs might not be doing enough. Instead, a better approach could be to stop the free radical reaction from happening in the first place.
Salomon explained that inflammation isn’t always a bad thing. The body needs it to heal wounds and fight off infection. It even plays a role in memory.
That’s why blocking leukotrienes completely could sometimes stop helpful processes, too. If pseudo leukotrienes are the real issue, then targeting them specifically could be safer and more effective.
To test their idea, Salomon and his team made pseudo leukotrienes in the lab. Then they looked for these molecules in urine samples from people with asthma. They found that people with asthma had four to five times more pseudo leukotrienes than people without asthma. The more severe the asthma, the higher the levels.
This means that pseudo leukotrienes could be used as a marker to tell how serious someone’s asthma is. It also means that we could monitor how well treatments are working by checking the levels of these molecules.
Next, the researchers want to find out if pseudo leukotrienes are involved in other lung diseases like RSV (a common virus in babies), bronchiolitis, and COPD. If they are, this could open up a whole new way of treating many types of breathing problems.
In short, this research challenges the old idea of what causes asthma and offers a promising new target for treatment. Instead of focusing on blocking inflammation after it starts, we might be able to stop it at the source—making life easier for the millions of people who struggle to breathe.
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The study is published in the Journal of Allergy and Clinical Immunology.
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